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Article type: Cover
1996 Volume 27 Issue 4 Pages
Cover13-
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Article type: Cover
1996 Volume 27 Issue 4 Pages
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Shuichi KOHRI, Yoshio SHIINA
Article type: Article
1996 Volume 27 Issue 4 Pages
513-519
Published: December 31, 1996
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The preparations of esophageal biopsies of 79 cases were tried to detect the human papilloma virus (HPV) DNA by in situ hybridization method. And we examined the rates and types of HPV DNA in each esophageal lesion, and discussed the relation between HPV infection and esophagal lesions. HPV DNA was detected 11 (13.9%) of 79 cases. In 11 cases of HPV DNA positive, two cases (2.5%) showed the types 16/18, nine cases (11.4%) showed the types 31/33/51 and no the types 6/11 was detected. The positive rate and type of HPV DNA in each esophageal lesion were as follows: three out of 19 cases (15.8%) of mild dysplasia showed the types 31/33/51, two out of 12 cases (16.7%) of moderate dysplasia showed the types 16/18 and 31/33/51, six out of 40 cases (15%) of patients with squamous cell carcinoma showed the types 16/18 for one and 31/33/51 for five. In patients of carcinoma, positive cell was showed in the atypia parts around cancer area and no positive cell in the cancer cells. No normal squamous epithelium of esophagus was detected. From the results, it is considered that the types 31/33/51 have a much higher affinity with esophageal epithelium and play some role in the esophageal dysplastic lesions was caused by HPV infection.
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Zenko NAKAMURA
Article type: Article
1996 Volume 27 Issue 4 Pages
521-531
Published: December 31, 1996
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The epileptogenic properties of the volatile anesthetics sevoflurane and isoflurane have not been investigated comparatively. The extent of spike activity was examined in 24 mentally and/or physically disabled patients, 12 with epilepsy and 12 without epilepsy. Electroencephalograms (EEGs) were recorded while the subjects were anesthetized with 1.0, 1.5 and then 2.0 MAC of sevoflurane or isoflurane during three ventilatory conditions: (A) 100% oxygen, ETCO_2=40mmHg, (B) 50% oxygen, 50% nitrous oxide, ETCO_2=40mmHg, and (C) 100% oxygen, ETCO_2=20mmHg. The background activity became significantly (p<0.05) slower as the MAC rose. The extent of spike activity increased significantly from 0.45±0.10/min under 1.0 MAC of sevoflurane to 1.21±0.55/min under 2.0 MAC of sevoflurane during ventilatory condition (A) in the epilepsy group, while no spike activity was observed in the non-epilepsy group. Supplementation with 50% nitrous oxide or hyperventilation significantly (p<0.05) suppressed the occurrence of spikes. In conclusion, sevoflurane has stronger epileptogenic properties in epileptic patients than isoflurane, but supplementation with nitrous oxide or hyperventilation counteracts the specific epileptogenic properties of this anesthetic agent.
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Haruyo TAKAKI
Article type: Article
1996 Volume 27 Issue 4 Pages
533-539
Published: December 31, 1996
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Thermal status during reperfusion after ischemia is a factor that affects the extent of neuronal injury following global ischemia. Anesthetics influence thermal status and seem to exert protective effect against ischemic neuronal injury through hypothermia. To elucidate the nature of this effect and to evaluate the protective effect of the newly developed volatile anesthetic, sevoflurane and the intravenous analgesics eptazocine on ischemic injury, we examined the relationship between brain temperature and neuronal injury after global ischemia. Mongolian gerbils were anesthetized with 1.5% halothane and oxygen. Both carotid arteries were exposed and occluded with threads for 5 min. Group I (n=6) was not given any anesthetic after occlusion. Group S (n=7) was given 2.8% sevoflurane for one hour. Group H (n=5) was given 1.2% halothane for one hour. Group E (n=5) was given eptazocine 10mg/kg intraperitoneally immediately after reperfusion. The animals was then perfusion-fixed with 4% paraformaldehyde and their brains were processed for histological examination. Pyramidal cell density of CA1 of hippocampus was 27±14/mm, 84±40/mm (p<0.05 vs Group I), 51±61/mm, 41±/mm in Group I, S, H, E, respectively (273±7/mm in normal brain). Brain temperature during repecfusion in Group S (35.3±0.7℃ at 30 min reperfusion) was significantly (p<0.05) lower than that in control Group I (38.2 ±1.3℃). Brain temperature during reperfusion is inversely related to the protective effect of anesthetics against neuronal injury in CA1. Sevoflurane has a protective effect of delayed neuronal through the prevention of hyperthermia during reperfusion.
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Chizuko IIJIMA
Article type: Article
1996 Volume 27 Issue 4 Pages
541-548
Published: December 31, 1996
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There is a significant difference in tolerance to ischemia between the retina and brain, although both use glutamate as a neurotransmitter. No study has yet made a comparison of glutamate release between the retina and brain following global ischemia. Using a dialysis electrode for real-time detection of glutamate, we examined the time course of glutamate release in the brain and the retina. Twelve Fischer rats were anesthetized with isoflurane. A dialysis probe for real-time glutamate measurement was implanted in the cerebral cortex though a cranial window placed on the right side of the temporal bone, and in the retina through the choroid. Laser Doppler flow probes were also projected on the cerebral cortex and the retina to confirm ischemia. Global ischemia was induced by ligation of both carotid arteries and hypotension down to 40mmHg by exsanguination for 20 min after heparinization. Reperfusion was established by reinfusion of blood and release of ligation for 60 min. Glutamate concentration in the retina was 166 ± 242μM/L which was significantly higher than that (81 ± 97μM/L, P <0.05) in the brain under control conditions. During global ischemia, the glutamate concentration increased to 449 ± 271μM/L (P <0.01) in the cortex, but decreased to 124 ± 155μM/ Lin the retina (P >0.05). Immediately after the start of reperfusion, glutamate in the cortex decreased rapidly to 136 ± 215μM/L, whereas that in the retina gradually increased to almost the control level (157 ± 215μM/L). There was a clearly opposite trend of glutamate release between the retina and cerebral cortex after ischemia. This difference in glutamate release might explain the difference in the tolerance of neurons to ischemia between the two organs.
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Hiroshi KATAHIRA
Article type: Article
1996 Volume 27 Issue 4 Pages
549-560
Published: December 31, 1996
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Free fatty acid (FFA) is usually increased in the sera of poorly controlled diabetic patients and its undesirable actions on glucose metabolism are reported. In the present study, the effect of FFA on insulin biosynthesis was investigated using isolated rat islets in vitro. Palmitic acid (PA) decreased insulin biosynthesis during the incubation of islets in the presence of 11 mM glucose in a dose and time related manner. Exposure of islets to 1.0 mM PA for 1 hour or 4 hours incubation suppressed insulin biosynthesis by 40 %. This inhibitory effect of PA was disappeared after eliminating PA from the incubation medium. To evaluate the effect of PA on preproinsulin transcription, the content of insulin mRNA in the incubated islets was measured by Northern blot analysis. PA did not affect insulin mRNA content during the 4 hours incubation period, suggesting that PA acts on the translational process of insulin synthesis. To further assess the mechanisms by which PA inhibits the insulin biosynthesis, the effect of PA on the contents of glucose transporter (GLUT2) protein and glucokinase protein were determined by immunoblot analysis. GLUT2 protein content did not change by addition of PA, however, the glucokinase protein content decreased about half fold. In agreement with this result, glucokinase activity reduced also about half fold by addition of PA. In conclusion, FFA suppresses glucose-induced insulin biosynthesis at the translational process partly mediated through decreased glucokinase activity.
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Article type: Appendix
1996 Volume 27 Issue 4 Pages
561-
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
563-564
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
564-565
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
566-567
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
567-568
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
569-570
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
570-571
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
571-572
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
573-574
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
574-575
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
576-577
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
577-578
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
578-579
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
580-581
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Article type: Article
1996 Volume 27 Issue 4 Pages
581-582
Published: December 31, 1996
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Article type: Article
1996 Volume 27 Issue 4 Pages
582-583
Published: December 31, 1996
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Article type: Article
1996 Volume 27 Issue 4 Pages
584-585
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
585-586
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
586-587
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
588-589
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
589-590
Published: December 31, 1996
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
590-591
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[in Japanese]
Article type: Article
1996 Volume 27 Issue 4 Pages
592-593
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Article type: Article
1996 Volume 27 Issue 4 Pages
593-594
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Article type: Article
1996 Volume 27 Issue 4 Pages
594-595
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Article type: Article
1996 Volume 27 Issue 4 Pages
596-597
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Article type: Article
1996 Volume 27 Issue 4 Pages
597-598
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Article type: Article
1996 Volume 27 Issue 4 Pages
599-600
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Article type: Article
1996 Volume 27 Issue 4 Pages
601-602
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Article type: Appendix
1996 Volume 27 Issue 4 Pages
603-
Published: December 31, 1996
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Article type: Appendix
1996 Volume 27 Issue 4 Pages
603-
Published: December 31, 1996
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Article type: Appendix
1996 Volume 27 Issue 4 Pages
603-
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Article type: Appendix
1996 Volume 27 Issue 4 Pages
App11-
Published: December 31, 1996
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Article type: Index
1996 Volume 27 Issue 4 Pages
i-iii
Published: December 31, 1996
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Article type: Appendix
1996 Volume 27 Issue 4 Pages
App12-
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Article type: Appendix
1996 Volume 27 Issue 4 Pages
App13-
Published: December 31, 1996
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Article type: Appendix
1996 Volume 27 Issue 4 Pages
App14-
Published: December 31, 1996
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Article type: Cover
1996 Volume 27 Issue 4 Pages
Cover15-
Published: December 31, 1996
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Article type: Cover
1996 Volume 27 Issue 4 Pages
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Published: December 31, 1996
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